How does positive pressure ventilation (PPV) decrease venous return?

Mechanism of Decreased Venous Return During Positive Pressure Ventilation

Positive pressure ventilation decreases venous return primarily by increasing intrathoracic pressure, which raises right atrial pressure and reduces the pressure gradient for venous return to the heart. 1

Primary Mechanisms

1. Altered Pressure Gradients

• Venous return is driven by the pressure gradient between the mean systemic filling pressure (upstream pressure in venous reservoir) and right atrial pressure (downstream pressure) 1
• Normal pressure gradient for venous return is only 4-8 mmHg 1
• Positive pressure ventilation increases pleural pressure (Ppl), which is transmitted to the right atrium
• This elevation in right atrial back pressure reduces the gradient for venous return throughout the ventilatory cycle 1

2. Transmission of Airway Pressure

• In normal subjects, approximately 50% of alveolar pressure changes are transmitted to pleural pressure 1
• In patients with stiffer lungs (e.g., ARDS), less pressure is transmitted to the pleural space 1
• When positive end-expiratory pressure (PEEP) is applied, the gradient for venous return is decreased throughout the entire ventilatory cycle 1

Secondary Mechanisms

1. Direct Compression of Great Veins

• At high lung volumes, hyperinflation can directly compress the thoracic vena cavae 2
• This creates a "vascular waterfall" effect where changes in right atrial pressure have no effect on venous return upstream of the compression point 2
• This effect varies by body position:
  • Most prominent in left lateral position
  • Least common in right lateral position
  • Variable in prone and supine positions 2

2. Effects on Pulmonary Vascular Resistance (PVR)

• Positive pressure ventilation can increase PVR, especially at high lung volumes 1
• When pleural pressure exceeds pulmonary venous pressure, microvascular collapse occurs (West zone 2 conditions) 1
• When pleural and interstitial pressures exceed pulmonary arterial pressure, blood flow is largely obstructed (West zone 1) 1
• Under these conditions, alveolar pressure becomes the outflow pressure for the right ventricle, increasing right ventricular afterload 1

Compensatory Mechanisms

• The body attempts to maintain venous return through:
  • Reflex decrease in vascular capacitance 1
  • Increased sympathetic tone
  • Abdominal pressure increases that partially offset the rise in right atrial pressure 3
  • In volume-loaded patients, increases in abdominal pressure can help maintain venous return despite positive pressure ventilation 3

Clinical Implications

• Positive pressure ventilation can cause significant hemodynamic compromise in hypovolemic patients 4
• In patients with asthma or obstructive lung disease, air trapping and auto-PEEP can further increase intrathoracic pressure, severely reducing venous return 1
• "Breath stacking" in patients with limited ability to exhale can lead to increases in intrathoracic pressure, decreases in venous return and coronary perfusion pressure, potentially causing cardiac arrest 1
• In patients with heart failure, the afterload-reducing effects of positive pressure ventilation on the left ventricle may actually improve cardiac output despite reduced venous return 4

Management Considerations

• In patients requiring positive pressure ventilation:
  • Ensure adequate volume status before initiating positive pressure ventilation 1
  • Use the lowest effective PEEP to maintain oxygenation 5
  • Consider lower tidal volumes (6-8 mL/kg) to minimize increases in intrathoracic pressure 5
  • Monitor for signs of decreased venous return (hypotension, tachycardia) 5
  • In severe asthma, consider brief disconnection from the ventilator or pauses in bag-mask ventilation with thoracic compression to relieve hyperinflation 1

Understanding these mechanisms is crucial for managing patients on positive pressure ventilation, especially those with pre-existing cardiovascular compromise or hypovolemia.